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Cancer Therapies HOL-emblem1-web.GIF (3556 bytes)

Second Protein Discovered To Target Her-2/Neu Cancers (February 2000)

Herceptin was approved in 1998 as a new anticancer drug for the treatment of breast cancers overexpressesing the Her-2/neu gene. Now researchers at M.D. Anderson Cancer Center, Texas, have discovered another protein that has the potential to inhibit tumors over-expressing this gene. (Reported in Nature Medicine.)

The Her-2/neu gene is activated when a protein (known as a transcription factor) binds to its promoter region. Mien-Chie Hung and colleagues discovered that for Her-2/neu, this activating protein is called PEA3, and comes from a family of proteins called 'Ets'. The scientists showed that PEA3 administration can prolong the survival of mice bearing human tumors and that it can block cancer formation in cells in culture.

Thus, PEA3 could be the basis for a new class of anti-cancer drugs that are effective against tumors over-expressing the Her-2/neu gene, and the findings also validates the idea that transcription factors from the Ets family could be used to switch off potentially cancer-causing genes. Good and bad news about gene therapy for brain cancer

Hope for patients with brain cancer, or glioma, has taken a cautious upswing in recent years with the advent of suicide-gene therapy. The therapy involves injection of an adenoviral vector (HSV1) carrying the gene for thymidine kinase (TK) into the brain, while the pro-drug ganciclovir is given systemically. When ganciclovir meets TK in brain cells, it is activated and destroys not only the cells carrying the gene but also surrounding cells due to a 'bystander effect.'

Pedro Lowenstein and colleagues at the University of Manchester, UK, have examined the long-term effects of this relatively new technique. They showed, in a rat model, that the treatment is very efficient, resulting in tumor destruction and the survival of 80-100% of animals for at least three months. However, examination of the brains of long-term survivors, revealed the presence of chronic brain inflammation and nerve cell destruction. They also found that many more neurons carried HSV1-TK than had been injected with the adenovirus.

These results have implications for ongoing clinical trials of HSV1-TK for glioma. Because many more cells than anticipated contain HSV1-TK, it may be possible to prolong ganciclovir administration and improve anti-tumor effects, but this should be weighed against the negative effects of inflammation and nerve cell destruction.

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